Evidence map›Paper›PMID 29187638›Full record

ArticleJournal of the Royal Society, Interface2017

Numb prevents a complete epithelial-mesenchymal transition by modulating Notch signalling.

Federico Bocci, Mohit K Jolly, Satyendra C Tripathi, Mitzi Aguilar, Samir M Hanash, Herbert Levine, José N Onuchic

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
8.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 114 citations in OpenAlex.

  1. Cancer spreading patterns based on epithelial-mesenchymal plasticity.Frontiers in cell and developmental biology · 2024
    Article
  2. Review
  3. Theoretical and computational tools to model multistable gene regulatory networks.Reports on progress in physics. Physical Society (Great Britain) · 2023
    Review
  4. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  5. The Intricate Notch Signaling Dynamics in Therapeutic Realms of Cancer.ACS pharmacology & translational science · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Frontiers in cell and developmental biology · 2022
    Review
  12. From COPD to Lung Cancer: Mechanisms Linking, Diagnosis, Treatment, and Prognosis.International journal of chronic obstructive pulmonary disease · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. The Most CommonCancers · 2021
    Article
  17. Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Federico BocciCenter for Theoretical Biological Physics, Rice University, Houston, TX, USA.ORCID 0000-0003-4302-9906
Mohit K JollyCenter for Theoretical Biological Physics, Rice University, Houston, TX, USA.
Satyendra C TripathiDepartment of Clinical Cancer Prevention, UT MD Anderson Cancer Center, Houston, TX, USA.
Mitzi AguilarDepartment of Clinical Cancer Prevention, UT MD Anderson Cancer Center, Houston, TX, USA.
Samir M HanashDepartment of Clinical Cancer Prevention, UT MD Anderson Cancer Center, Houston, TX, USA shanash@mdansderon.org.
Herbert LevineCenter for Theoretical Biological Physics, Rice University, Houston, TX, USA hl34@rice.edu.
José N OnuchicCenter for Theoretical Biological Physics, Rice University, Houston, TX, USA jnonuchic@rice.edu.
Center for Theoretical Biological Physics · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) plays key roles during embryonic development, wound healing and cancer metastasis. Cells in a partial EMT or hybrid epithelial/mesenchymal (E/M) phenotype exhibit collective cell migration, forming clusters of circulating tumour cells-the primary drivers of metastasis. Activation of cell-cell signalling pathways such as Notch fosters a partial or complete EMT, yet the mechanisms enabling cluster formation remain poorly understood. Using an integrated computational-experimental approach, we examine the role of Numb-an inhibitor of Notch intercellular signalling-in mediating EMT and clusters formation. We show via an mathematical model that Numb inhibits a full EMT by stabilizing a hybrid E/M phenotype. Consistent with this observation, knockdown of Numb in stable hybrid E/M cells H1975 results in a full EMT, thereby showing that Numb acts as a brake for a full EMT and thus behaves as a 'phenotypic stability factor' by modulating Notch-driven EMT. By generalizing the mathematical model to a multi-cell level, Numb is predicted to alter the balance of hybrid E/M versus mesenchymal cells in clusters, potentially resulting in a higher tumour-initiation ability. Finally, Numb correlates with a worse survival in multiple independent lung and ovarian cancer datasets, hence confirming its relationship with increased cancer aggressiveness.

Indexed as

Epithelial-Mesenchymal TransitionCell CommunicationCell LineCell MovementComputational BiologyHumansMembrane ProteinsModels, TheoreticalNerve Tissue ProteinsReceptors, NotchMembrane ProteinsNerve Tissue ProteinsNUMB protein, humanReceptors, Notchcirculating tumour cells clustersepithelial–mesenchymal transitionhybrid epithelial/mesenchymal phenotypeNotch signallingNumb

Identifiers

PMID29187638
PMCPMC5721160
OpenAlexW2770361061

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.